Inducible transcription factor expression in a cell culture model of apoptosis
We have developed a model of nerve cell death based on the toxicity of okadaic acid, a compound that triggers apoptosis in PC12 cells via a protein synthesis-dependent mechanism. The cell death process is accompanied by induction of JunB, c-Jun, JunD and Fos proteins. Phosphorylation-specific antibo...
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| Veröffentlicht in: | Brain research. Molecular brain research. 1999-03, Vol.66 (1), p.211-216 |
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| container_title | Brain research. Molecular brain research. |
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| creator | Woodgate, A Walton, M MacGibbon, G.A Dragunow, M |
| description | We have developed a model of nerve cell death based on the toxicity of okadaic acid, a compound that triggers apoptosis in PC12 cells via a protein synthesis-dependent mechanism. The cell death process is accompanied by induction of JunB, c-Jun, JunD and Fos proteins. Phosphorylation-specific antibodies were used to demonstrate that c-Jun is phosphorylated at serine 63 and serine 73. Electrophoretic gel mobility shift and pAP1-Luc luciferase assays showed that expression of ITFs is associated with increases in AP-1 binding and in AP-1 transcriptional activity. In addition, dose response and time course studies provided strong correlative evidence that Fos and Jun proteins are involved in the apoptotic death cascades. Thus, this model provides a useful system to investigate the role of inducible transcription factor proteins in apoptosis. |
| doi_str_mv | 10.1016/S0169-328X(99)00027-3 |
| format | Article |
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The cell death process is accompanied by induction of JunB, c-Jun, JunD and Fos proteins. Phosphorylation-specific antibodies were used to demonstrate that c-Jun is phosphorylated at serine 63 and serine 73. Electrophoretic gel mobility shift and pAP1-Luc luciferase assays showed that expression of ITFs is associated with increases in AP-1 binding and in AP-1 transcriptional activity. In addition, dose response and time course studies provided strong correlative evidence that Fos and Jun proteins are involved in the apoptotic death cascades. Thus, this model provides a useful system to investigate the role of inducible transcription factor proteins in apoptosis.</description><identifier>ISSN: 0169-328X</identifier><identifier>EISSN: 1872-6941</identifier><identifier>DOI: 10.1016/S0169-328X(99)00027-3</identifier><identifier>PMID: 10095097</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Ageing, cell death ; Alzheimer's disease ; Animals ; AP-1 ; Apoptosis - drug effects ; Apoptosis - physiology ; Biological and medical sciences ; c-Jun ; Cell physiology ; CREB ; Cyclic AMP Response Element-Binding Protein - genetics ; Cyclic AMP Response Element-Binding Protein - metabolism ; DNA Probes ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Gene Expression - genetics ; Molecular and cellular biology ; Neurons - chemistry ; Neurons - cytology ; Neurons - physiology ; Okadaic acid ; Okadaic Acid - pharmacology ; Pancreatitis-Associated Proteins ; PC12 cell ; PC12 Cells ; Phosphorylation ; Proto-Oncogene Proteins c-jun - genetics ; Proto-Oncogene Proteins c-jun - metabolism ; Rats ; Transcription Factor AP-1 - genetics ; Transcription Factor AP-1 - metabolism</subject><ispartof>Brain research. Molecular brain research., 1999-03, Vol.66 (1), p.211-216</ispartof><rights>1999</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999 Published by Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-b6285c3d50f71e90523c492f7b85760292a965ae72e395d974fc4e31677cc8313</citedby><cites>FETCH-LOGICAL-c421t-b6285c3d50f71e90523c492f7b85760292a965ae72e395d974fc4e31677cc8313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1779215$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10095097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Woodgate, A</creatorcontrib><creatorcontrib>Walton, M</creatorcontrib><creatorcontrib>MacGibbon, G.A</creatorcontrib><creatorcontrib>Dragunow, M</creatorcontrib><title>Inducible transcription factor expression in a cell culture model of apoptosis</title><title>Brain research. Molecular brain research.</title><addtitle>Brain Res Mol Brain Res</addtitle><description>We have developed a model of nerve cell death based on the toxicity of okadaic acid, a compound that triggers apoptosis in PC12 cells via a protein synthesis-dependent mechanism. The cell death process is accompanied by induction of JunB, c-Jun, JunD and Fos proteins. Phosphorylation-specific antibodies were used to demonstrate that c-Jun is phosphorylated at serine 63 and serine 73. Electrophoretic gel mobility shift and pAP1-Luc luciferase assays showed that expression of ITFs is associated with increases in AP-1 binding and in AP-1 transcriptional activity. In addition, dose response and time course studies provided strong correlative evidence that Fos and Jun proteins are involved in the apoptotic death cascades. Thus, this model provides a useful system to investigate the role of inducible transcription factor proteins in apoptosis.</description><subject>Ageing, cell death</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>AP-1</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>c-Jun</subject><subject>Cell physiology</subject><subject>CREB</subject><subject>Cyclic AMP Response Element-Binding Protein - genetics</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>DNA Probes</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression - genetics</subject><subject>Molecular and cellular biology</subject><subject>Neurons - chemistry</subject><subject>Neurons - cytology</subject><subject>Neurons - physiology</subject><subject>Okadaic acid</subject><subject>Okadaic Acid - pharmacology</subject><subject>Pancreatitis-Associated Proteins</subject><subject>PC12 cell</subject><subject>PC12 Cells</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-jun - genetics</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Rats</subject><subject>Transcription Factor AP-1 - genetics</subject><subject>Transcription Factor AP-1 - metabolism</subject><issn>0169-328X</issn><issn>1872-6941</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu1DAQhi1ERbeFRwD5gFA5BDx2HMenClWFrrSCAyBxs7yTiWSUjYOdVO3bN2lWwK2XGWn0zcyvj7HXID6AgOrj97nYQsn614W174UQ0hTqGdtAbWRR2RKes81f5JSd5fx7hqAGeMFOQQirhTUb9nXbNxOGfUd8TL7PmMIwhtjz1uMYE6e7IVHOyyT03HOkruM4deOUiB9iQx2PLfdDHMaYQ37JTlrfZXp17Ofs5-frH1c3xe7bl-3Vp12BpYSx2Fey1qgaLVoDZIWWCksrW7OvtamEtNLbSnsykpTVjTVliyUpqIxBrBWoc_ZuvTuk-GeiPLpDyEs231OcsgMDVst6AfUKYoo5J2rdkMLBp3sHwi0i3aNIt1hy1rpHkU7Ne2-OD6b9gZr_tlZzM_D2CPiMvmtneRjyP84YK0HP2OWK0WzjNlByGQP1SE1IhKNrYngiyQPOJ49M</recordid><startdate>19990320</startdate><enddate>19990320</enddate><creator>Woodgate, A</creator><creator>Walton, M</creator><creator>MacGibbon, G.A</creator><creator>Dragunow, M</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>19990320</creationdate><title>Inducible transcription factor expression in a cell culture model of apoptosis</title><author>Woodgate, A ; Walton, M ; MacGibbon, G.A ; Dragunow, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-b6285c3d50f71e90523c492f7b85760292a965ae72e395d974fc4e31677cc8313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Ageing, cell death</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>AP-1</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>c-Jun</topic><topic>Cell physiology</topic><topic>CREB</topic><topic>Cyclic AMP Response Element-Binding Protein - genetics</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>DNA Probes</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>Gene Expression - genetics</topic><topic>Molecular and cellular biology</topic><topic>Neurons - chemistry</topic><topic>Neurons - cytology</topic><topic>Neurons - physiology</topic><topic>Okadaic acid</topic><topic>Okadaic Acid - pharmacology</topic><topic>Pancreatitis-Associated Proteins</topic><topic>PC12 cell</topic><topic>PC12 Cells</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-jun - genetics</topic><topic>Proto-Oncogene Proteins c-jun - metabolism</topic><topic>Rats</topic><topic>Transcription Factor AP-1 - genetics</topic><topic>Transcription Factor AP-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Woodgate, A</creatorcontrib><creatorcontrib>Walton, M</creatorcontrib><creatorcontrib>MacGibbon, G.A</creatorcontrib><creatorcontrib>Dragunow, M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Brain research. Molecular brain research.</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Woodgate, A</au><au>Walton, M</au><au>MacGibbon, G.A</au><au>Dragunow, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inducible transcription factor expression in a cell culture model of apoptosis</atitle><jtitle>Brain research. Molecular brain research.</jtitle><addtitle>Brain Res Mol Brain Res</addtitle><date>1999-03-20</date><risdate>1999</risdate><volume>66</volume><issue>1</issue><spage>211</spage><epage>216</epage><pages>211-216</pages><issn>0169-328X</issn><eissn>1872-6941</eissn><abstract>We have developed a model of nerve cell death based on the toxicity of okadaic acid, a compound that triggers apoptosis in PC12 cells via a protein synthesis-dependent mechanism. The cell death process is accompanied by induction of JunB, c-Jun, JunD and Fos proteins. Phosphorylation-specific antibodies were used to demonstrate that c-Jun is phosphorylated at serine 63 and serine 73. Electrophoretic gel mobility shift and pAP1-Luc luciferase assays showed that expression of ITFs is associated with increases in AP-1 binding and in AP-1 transcriptional activity. In addition, dose response and time course studies provided strong correlative evidence that Fos and Jun proteins are involved in the apoptotic death cascades. Thus, this model provides a useful system to investigate the role of inducible transcription factor proteins in apoptosis.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10095097</pmid><doi>10.1016/S0169-328X(99)00027-3</doi><tpages>6</tpages></addata></record> |
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| subjects | Ageing, cell death Alzheimer's disease Animals AP-1 Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences c-Jun Cell physiology CREB Cyclic AMP Response Element-Binding Protein - genetics Cyclic AMP Response Element-Binding Protein - metabolism DNA Probes Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Gene Expression - genetics Molecular and cellular biology Neurons - chemistry Neurons - cytology Neurons - physiology Okadaic acid Okadaic Acid - pharmacology Pancreatitis-Associated Proteins PC12 cell PC12 Cells Phosphorylation Proto-Oncogene Proteins c-jun - genetics Proto-Oncogene Proteins c-jun - metabolism Rats Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism |
| title | Inducible transcription factor expression in a cell culture model of apoptosis |
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